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首页> 外文期刊>Journal of vascular research >The GPER1 Agonist G-1 Attenuates Endothelial Cell Proliferation by Inhibiting DNA Synthesis and Accumulating Cells in the S and G2 Phases of the Cell Cycle.
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The GPER1 Agonist G-1 Attenuates Endothelial Cell Proliferation by Inhibiting DNA Synthesis and Accumulating Cells in the S and G2 Phases of the Cell Cycle.

机译：GPER1激动剂G-1通过抑制DNA合成并在细胞周期的S和G2期积聚细胞来减轻内皮细胞的增殖。

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G protein-coupled receptor 30 (GPR30) or G protein-coupled estrogen receptor 1 (GPER1) is expressed in the vasculature, but the importance of vascular GPER1 remains to be clarified. Here we investigate effects of the GPER1 agonist G-1 on endothelial cell proliferation using mouse microvascular endothelial bEnd.3 cells. The bEnd.3 cells express mRNA for GPER1. The bEnd.3 cells expressed both ERalpha and ERbeta immunoreactivities. Treatment with G-1 reduced DNA synthesis and cell number with IC(50) values of about 2 muM. GPER1 siRNA prevented G-1-induced attenuation of DNA synthesis. G-1 accumulated cells in S and G2 phases of the cell cycle, suggesting that G-1 blocks transition between G2 and M. G-1 had no effect on DNA synthesis in COS-7 cells only weakly expressing GPER1 mRNA. 17beta-Estradiol had no effect on DNA synthesis in physiological concentrations (nM). The ER blocker ICI182780 reduced DNA synthesis with similar potency as G-1. Treatment with the ERK/MAP kinase inhibitor PD98059 had no effect on G-1-induced attenuation of DNA synthesis. G-1- induced antiproliferation was observed not only in bEnd.3 cells but also in human umbilical vein endothelial cells and HMEC-1 endothelial cells. We conclude that the GPER1 agonist G-1 attenuates endothelial cell proliferation via inhibition of DNA synthesis and by accumulation of cells in S and G2.
机译：G蛋白偶联受体30（GPR30）或G蛋白偶联雌激素受体1（GPER1）在脉管系统中表达，但血管GPER1的重要性仍有待阐明。在这里，我们使用小鼠微血管内皮bEnd.3细胞研究GPER1激动剂G-1对内皮细胞增殖的影响。 bEnd.3细胞表达GPER1的mRNA。 bEnd.3细胞同时表达ERalpha和ERbeta免疫反应性。用G-1处理可降低DNA合成和细胞数量，IC（50）值约为2μM。 GPER1 siRNA阻止了G-1诱导的DNA合成衰减。 G-1在细胞周期的S和G2期积聚细胞，表明G-1阻止了G2和M之间的过渡。G-1对仅弱表达GPER1 mRNA的COS-7细胞的DNA合成没有影响。 17β-雌二醇在生理浓度（nM）下对DNA合成没有影响。 ER阻滞剂ICI182780可以以与G-1相似的效价降低DNA合成。用ERK / MAP激酶抑制剂PD98059处理对G-1诱导的DNA合成衰减没有影响。 G-1-诱导的抗增殖不仅在bEnd.3细胞中观察到，而且在人脐静脉内皮细胞和HMEC-1内皮细胞中也观察到。我们得出的结论是，GPER1激动剂G-1通过抑制DNA合成以及通过在S和G2中积累细胞来减弱内皮细胞的增殖。

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